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Use of a Hanging-weight System for Isolated Renal Artery Occlusion

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THE ETIOLOGY OF HYPERTENSION DUE TO COMPLETE RENAL ISCHEMIA.

M Prinzmetal¹, H A Lewis, S D Leo

¹Department of Physiology and Medicine of the University of Southern California, School of Medicine, and the Research Laboratory of the Cedars of Lebanon Hospital, Los Angeles.

The Journal of Experimental Medicine

|October 30, 2009

Summary

Totally ischemic cat kidneys produce a pressor substance, identified as renin, which causes hypertension upon reperfusion. This substance, formed during ischemia, reacts with plasma to create a heat-stable pressor agent.

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Area of Science:

Renal Physiology
Hypertension Research
Biochemistry

Background:

Ischemia in organs can lead to the production of vasoactive substances.
The role of the kidney in producing pressor substances during ischemic events requires further elucidation.
Understanding the mechanisms of post-ischemic hypertension is crucial for clinical management.

Purpose of the Study:

To identify and characterize the pressor substance present in perfusates of ischemic cat kidneys.
To determine the origin and role of this substance in causing hypertension following renal ischemia.
To investigate the relationship between this pressor substance and renin.

Main Methods:

Perfusion of totally ischemic and normal cat kidneys, hind limbs, and gravid uteri.
Analysis of perfusates for pressor activity and comparison with known vasoactive substances.
Incubation of perfusates with plasma and assessment of the resulting pressor substance.
Extraction of pressor material from released and unreleased ischemic kidneys.

Main Results:

A pressor substance, absent in normal tissues, was found in perfusates of ischemic cat kidneys.
This substance originates in the kidney due to complete ischemia and causes hypertension upon reperfusion.
Evidence strongly suggests the pressor principle is renin, based on its properties (heat lability, tachyphylaxis, reaction with plasma to form a heat-stable substance) and comparison with epinephrine.

Conclusions:

Complete renal ischemia in cats generates a pressor substance, presumed to be renin.
This renin contributes to post-ischemic hypertension by forming a heat-stable pressor agent (angiotonin/hypertensin) with plasma during ischemia.
A method was developed to test substances affecting renin production in the ischemic kidney.